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equine endocrine

endrocrine

QuestionAnswer
EQUINE CUSHING’S DISEASE known as PARS PITUITARY INTERMEDIA DYSFUNCTION
Pars Pituitary intermedia dysfunction Clinical syndrome associated with hirsutism, polydipsia, polyruia, and hyperglycemia
All breeds and types of horses affected pars pituitary intermedia dysfunction
Cushings is a disease of middle-aged / older horses (> 15 years of age)
The diffuse physical enlargement of the pars intermedia results from decreased dopaminergic innervation from the hypothalamus
It is the loss of dopaminergic inhibition which leads to clinical signs of disease cushings
Without dopaminergic inhibition melanotrope hormone release is increased
Without dopaminergic inhibition melanotrope hormone release is increased This is evidenced by increased and uncontrolled secretion of endorphin (END),melanotropin (MSH), and adrenocorticotropin hormone (ACTH) from proopiomelanocortin peptides in afflicted animals
Secondary adrenocortical involvement results from the secretion of these pituitary hormones
Sequela of the excess circulating glucocorticoids, physical destruction of the pars nervosa, and, likely the direct peripheral action of the pituitary proopiomelanocortin (POMC)-derived peptides
Average age of affected horses is 19 years
No sex predilection equine cushings
Hirsutism long, thick, curly coat that fails to shed
It is the most common clinical sign observed hirsutism
Change in shedding behavior and the appearance of guard hairs beneath the mandible, along the chin or distal limbs in the summer may be an early indication of PPID and may be recognized by owners prior to full-body coat hirsuitism
Chronic or recurrent acute laminitis is common and may be the only presenting complaint PPID
Leading cause of euthanasia in horses with PPID
Polyuria and polydipsia are common PPID
Destruction of the pars nervosa by the enlarged pars intermedia leads to decreased secretion of arginine vasopressin (AVP), originally known as antidiuretic hormone (ADH)
Hyperglycemia also promotes osmotic diuresis
Hyperhidrosis is observed in many horses with PPID
Equine sweat glands are under adrenergic control
Neutrophilia with concurrent lymphopenia is commonly observed
Hyperglycemia and insulin-resistance is present in many cases
Definitive diagnostic tests include Low-dose dexamethasone suppression test Overnight protocol
Draw pre-dexamethasone blood sample at 5 pm, then administer dexamethasone
Draw post-dex blood sample 19 hours later
Normal horses should have good cortisol suppression (<1g/dl) 19 hours after administration of dexamethasone
Overnight test is excellent for screening
Seasonal variation – August / September months may reveal abnormal results (false positive)
Most striking necropsy lesion is pituitary enlargement; attributable to diffuse, adenomatous hyperplasia of the pars intermedia
Treatment requires fastidious management protocols
Excellent husbandry and feeding practices and careful management of secondary complications, such as chronic infections and laminitis
The use of a dopaminergic agonist has been associated with modest declines in POMC peptides as well as improvement in clinical signs
Pergolide is a long-acting dopaminergic agonist
Pergolide Side effects (diarrhea, colic, anorexia) are dose dependent
Cyproheptidine is a drug with anti-serotonergic activity and has been used with limited success
Prognosis:Affected horses that are euglycemic have an excellent long-term prognosis with appropriate management
Horses that are mildly hyperglycemic also generally have a good prognosis but can be more susceptible than euglycemic animals to intercurrent infectious problems
Horses that are moderately to severely hyperglycemic (>275 mg/dl) have a guarded prognosis
EQUINE METABOLIC SYNDROME Similar to human metabolic syndrome in that horses have regional adiposity (deposition of fat along the crest of the neck, tail head, withers) and insulin resistance
However, equine metabolic syndrome is unique
Other features of human metabolic syndrome have not been found with EMS such as hypertension, abdominal adiposity, and microalbuminemia
Horses present with obesity (excessive fat accumulation in the body) and a body condition score > 7 / 9 (Henneke scale 1-9), as well as insulin resistance and subclinical / clinical laminitis equine metabolic syndrome
Genetics appear to be associated with the development of insulin resistance and obesity
Ponies tend to be more insulin resistant than horses, although some horse breeds are more prone Morgans > Arabs > Fjords
These horses are typically known as Easy-keepers in that very little feed keeps horses in heavy body condition
Environmental factors also play a role, diet and exercise equine metabolic syndrome
EMS is a disease of adult horses (> 5 years) with no sex predilection
Diagnosis of EMS may be made by documenting resting hyperinsulinemia
Insulin > 20U/mL suggests insulin resistance
Insulin > 30 U/mL defines hyperinsulinemia
Diagnosis may also be confirmed using a combined glucose-insulin test
Field test to detect insulin resistance,collect baseline blood glucose,dminister 150 mg/kg 50pct dextrose IV,Follow with 0
10 U/kg insulin IV,Documentation of elevated blood glucose above baseline for >45 minutes is indicative of insulin resistance
EMS management requires diet and exercise,Weight loss is critical, Remove CHO from diet
In EMS Monitor non-structural CHO in hay Should be < 12pct,Soaking hay prior to feeding decreaes CHO
Feed grass hay for EMS 1
5 – 2
0pct of body weight / day based on goal weight
Restrict pasture grazing and encourage use of grazing muzzle
Exercise is important in EMS but may be difficult with clinical laminitis
Once the EMS condition is stabilized hand-walking is encouraged
Swimming is ideal for EMS
Additional therapy: Levothyroxine for EMS May lower body weight / improve insulin sensitivity
Prescribe until reach ideal body weight Levothyroxine
Do not use for >6 months Levothyroxine
Equine hypothyroidism is poorly understood and many theories / etiologies have yet to be substantiated (ie laminitis,obesity,rhabdomyolysis,anhidrosis)
Hypothyroidism should be considered in the differential of any horse presenting with a history of lethargy, poor exercise tolerance, or muscular problems
It may be difficult to confirm the diagnosis due to challenges of performing testing in the field hypothyroidism
The diagnosis of hypothyroidism is most commonly based on low serum concentrations of total T4 and T3, but may be more definitively diagnosed following TSH / TRH stimulation tests
Although some will suggest response to thyroid supplementation is diagnostic the placebo affect may conflict interpretation
Endophyte alkaloids (produced by a symbiotic fungus living on the fescue grass) act as dopamine agonists
TSH is inhibited by dopamine – as a result, it has been suggested that fescue consumption can lead to hypothyroidism
May see prolonged gestation and agalactia fescue hypothyroidism
Treatment fescue hypothyroidism domperidone (dopamine antagonist)
At birth, the normal foal has plasma concentrations of thyroxine (T4) and triiodothyronine (T3) 10-20 times greater than the adult and also greater than reported in any other species
Hyperplastic goiter in neonates is the most common thyroid disorder in the horse
It is thought to result from the mare’s excess iodine consumption or plant goitrogens during gestation hyperplastic goiter in neonates
An additional syndrome of dysmaturity (prolonged gestation), mandibular pragnathism and incomplete ossification has also been reported in foals of the western USA and Canada
Caution is warranted with thyroid supplementation without confirmation of diagnosis, as the associated health risks in horses is largely unexplored
In humans, health risks include decreased bone density and increased risk of atrial fibrillation, myocardial infarction, and congestive heart failure
Thyroid adenomas relatively common and may be easily palpable as enlarged gland in the cranial neck alongside the proximal trachea in the adult horse
Most thyroid tumors are benign and nonfunctional and thyroid hormones remain WNL
Treatment is unnecessary unless the mass becomes large enough to compress the respiratory and/or ailmentary tracts thyroid adenoma
If thyroidectomy is required, appropriate thyroid hormone supplementation is warranted
Diabetes insipidus results from decreased release of ADH from the posterior pituitary
The most common cause of decreased ADH release in the horse is posterior pituitary destruction secondary to pars intermedia enlargement, but rare cases of primary diabetes insipidus have been reported
Diabetes insipidus Clinical presentation PU/PD in an otherwise normal animal, azotemia is NOT present
Diabetes insipidus Urine specific gravity < 1
010 and the patient fails to concentrate urine on a water deprivation test
Psychogenic polydypsia syndrome is observed as a stable vice in some horses
These patients are able to concentrate urine (> 1
025) when they are subjected to water deprivation test pshychogenic polydypsia
Nutritional hyperparathyroidism (Big head / Bran disease / Miller’s disease) was formerly the most common cause of hyperparathyroidism in the horse
This condition has become rare as knowledge of proper equine nutrition has become more widespread nutritional hyperparathyroidism
A relative calcium deficiency secondary to excess dietary phosphorus lead to the clinical signs of Big Head disease
Clinical signs include facial bone enlargement, difficulty in mastication due to bone loss, fractures of the molars, spontaneous long bone fractures may occur, unthriftiness, shifting lameness and physitis / limb deformities in young animals Big Head disease
Upper airway noise may be heard due to narrowing of the nasal passages with bony remodeling
Elevated phosphorus and decreased calcium lead to hyperplasia of the parathyroid gland
PTH secretion inhibits Vitamin D synthesis, increases bone resorption and bone loss (primarily of bones in the face)
The bone loss is replaced by un-mineralized connective tissue
Most patients remain normocalcemic as this disease is very slowly progressive, calcium levels are maintained
Radiographs are helpful only if >30pct of mineral loss has occurred
Treatment involves elimination of grain in the diet as well as feeds that contain excess oxalates
Supplementation of calcium is warranted, typically in the form of calcium carbonate (limestone)
The ideal ratio is Ca:P between 3:1 and 4:1 for supplementation therapy
Recovery is possible, but requires many months and some bony abnormalities may not be resolved
Vitamin D toxicosis can result from overzealous administration of vitamin D containing nutritional supplements or ingestion of plants with leaves that have vitamin D like biologic activity
Example = Cestrum diurnum plants with leaves that have vitamin D like biologic activity
These horses have elevated serum calcium with normal serum phosphorus vitamin D toxicosis
Vitamin D toxicosis Pathologic calcification of soft tissue is widespread in arteries, tendons, and ligaments
Prognosis is poor Vitamin D toxicosis once pathologic calcification of soft tissue is present
Created by: alljacks